Research ended on promising Alzheimer’s drug

It is not surprising that finding a cure or effective treatment for Alzheimer’s disease is a high priority for medical researchers. After all, the Alzheimer’s Society has predicted that by the year 2025, more than one million people in the UK will be afflicted by dementia.

News that late-stage trials of a promising new drug to treat the condition have been abandoned is, therefore, disappointing for many. Verubecestat has been declared to have no positive effect on the test subjects and will not go any further forward towards being marketed.

This is not the first time that a drug representing hope for the future in the world of Alzheimer’s has seen its trials cancelled. In November 2016, solanezumab had its tests halted, despite also being in the late stages of its trials.

It had been hoped that moderate forms of Alzheimer’s disease could be treated with an injection of the drug, but its US developers found this was not the case. The sudden stopping of two seemingly promising treatments in close succession has come as quite a blow to the research community.

Bart De Strooper, director of the Dementia Research Institute at University College London, said that researchers really need to start thinking in a different way to try and make some progress.

He added: “Researchers have had too simplistic an approach to dementia. What is emerging is that these brain diseases are highly complex, with many processes, not just one. We need to make our research more nuanced.”

The principle that the development of solanezumab and verubecestat were both based on was the fact that they inhibit the amyloid proteins that form sticky clumps in the brains of Alzheimer’s sufferers. Researchers have been focusing their efforts on these proteins for many years, but it could be that this will change in future.

Another drug, AZD3293, which uses the same approach, is currently being trialled and is not expected to have its results released until May 2019. Only time will tell if it has a better outcome than its two predecessors, but it will need to be significantly different to prove successful where others failed.

Experts in the field are trying not to despair entirely at this latest development, with many suggesting a simple reason for the drugs not working. That is that by the time symptoms of dementia arise, it is too late to target amyloid plaques that have already formed.

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